Ginsenoside Metabolite Compound K Alleviates Adjuvant-Induced Arthritis by Suppressing T Cell Activation

Jingyu Chen, Huaxun Wu, Qingtong Wang, Yan Chang, Kangkang Liu, Shasha Song, Pingfan Yuan, Jingjing Fu, Wuyi Sun, Qiong Huang, Lihua Liu, Yujing Wu, Yunfang Zhang, Aiwu Zhou, Wei Wei

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Ginsenoside metabolite compound K (CK) is the degradation product of ginsenosides in the intestine by bacteria and has many pharmacological activities including anti-inflammatory effects. Rheumatoid arthritis (RA) is an inflammatory and autoimmune disease characterized by chronic synovial inflammation and articular damage in multiple joints. However, the effect of CK on RA remains unclear. In this study, the effect of CK on adjuvant arthritis (AA) and the underlying mechanisms that focused on T cell activation were investigated. Complete Freund’s adjuvant was used to induce AA rats. After the onset of arthritis, rats were given CK (10, 40, and 160 mg/kg) or MTX (0.5 mg/kg). To evaluate the severity of arthritis, arthritis index and paw swelling were evaluated every 3 days. Histopathology of joint and spleen were assayed. Subsets of T cells including CD4 + CD62L+ (naïve T cells), CD4 + CD25+ (activated T cells), and CD4 + CD25 + Foxp3+ cells (Treg) and CD25 expression were assayed by flow cytometry. Proliferation of T cell was evaluated by 3H-TdR. IL-2 level was assayed by ELISA. We found that CK attenuated arthritis index and paw swelling, restored the histopathological change of joint and spleen, downregulated the percentage of activated T cells, and upregulated naïve T cells and Treg cells in spleen. CK significantly suppressed T cell activation (as indicated by T cell proliferation, CD25 expression, and IL-2 production). In conclusion, our results suggest that CK alleviates autoimmune arthritis by suppressing T cell activation.

Original languageEnglish (US)
Pages (from-to)1608-1615
Number of pages8
JournalInflammation
Volume37
Issue number5
DOIs
StatePublished - Jan 1 2014
Externally publishedYes

Fingerprint

Experimental Arthritis
T-Lymphocytes
Arthritis
Joints
Spleen
Regulatory T-Lymphocytes
Interleukin-2
Rheumatoid Arthritis
Ginsenosides
ginsenoside M1
Freund's Adjuvant
T-Lymphocyte Subsets
Autoimmune Diseases
Intestines
Flow Cytometry
Anti-Inflammatory Agents
Down-Regulation
Enzyme-Linked Immunosorbent Assay
Cell Proliferation
Pharmacology

Keywords

  • adjuvant-induced arthritis
  • CD25
  • ginsenoside metabolite compound K
  • IL-2
  • regulatory T cells
  • T cell activation

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Ginsenoside Metabolite Compound K Alleviates Adjuvant-Induced Arthritis by Suppressing T Cell Activation. / Chen, Jingyu; Wu, Huaxun; Wang, Qingtong; Chang, Yan; Liu, Kangkang; Song, Shasha; Yuan, Pingfan; Fu, Jingjing; Sun, Wuyi; Huang, Qiong; Liu, Lihua; Wu, Yujing; Zhang, Yunfang; Zhou, Aiwu; Wei, Wei.

In: Inflammation, Vol. 37, No. 5, 01.01.2014, p. 1608-1615.

Research output: Contribution to journalArticle

Chen, J, Wu, H, Wang, Q, Chang, Y, Liu, K, Song, S, Yuan, P, Fu, J, Sun, W, Huang, Q, Liu, L, Wu, Y, Zhang, Y, Zhou, A & Wei, W 2014, 'Ginsenoside Metabolite Compound K Alleviates Adjuvant-Induced Arthritis by Suppressing T Cell Activation', Inflammation, vol. 37, no. 5, pp. 1608-1615. https://doi.org/10.1007/s10753-014-9887-0
Chen, Jingyu ; Wu, Huaxun ; Wang, Qingtong ; Chang, Yan ; Liu, Kangkang ; Song, Shasha ; Yuan, Pingfan ; Fu, Jingjing ; Sun, Wuyi ; Huang, Qiong ; Liu, Lihua ; Wu, Yujing ; Zhang, Yunfang ; Zhou, Aiwu ; Wei, Wei. / Ginsenoside Metabolite Compound K Alleviates Adjuvant-Induced Arthritis by Suppressing T Cell Activation. In: Inflammation. 2014 ; Vol. 37, No. 5. pp. 1608-1615.
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AU - Wu, Huaxun

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AU - Chang, Yan

AU - Liu, Kangkang

AU - Song, Shasha

AU - Yuan, Pingfan

AU - Fu, Jingjing

AU - Sun, Wuyi

AU - Huang, Qiong

AU - Liu, Lihua

AU - Wu, Yujing

AU - Zhang, Yunfang

AU - Zhou, Aiwu

AU - Wei, Wei

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N2 - Ginsenoside metabolite compound K (CK) is the degradation product of ginsenosides in the intestine by bacteria and has many pharmacological activities including anti-inflammatory effects. Rheumatoid arthritis (RA) is an inflammatory and autoimmune disease characterized by chronic synovial inflammation and articular damage in multiple joints. However, the effect of CK on RA remains unclear. In this study, the effect of CK on adjuvant arthritis (AA) and the underlying mechanisms that focused on T cell activation were investigated. Complete Freund’s adjuvant was used to induce AA rats. After the onset of arthritis, rats were given CK (10, 40, and 160 mg/kg) or MTX (0.5 mg/kg). To evaluate the severity of arthritis, arthritis index and paw swelling were evaluated every 3 days. Histopathology of joint and spleen were assayed. Subsets of T cells including CD4 + CD62L+ (naïve T cells), CD4 + CD25+ (activated T cells), and CD4 + CD25 + Foxp3+ cells (Treg) and CD25 expression were assayed by flow cytometry. Proliferation of T cell was evaluated by 3H-TdR. IL-2 level was assayed by ELISA. We found that CK attenuated arthritis index and paw swelling, restored the histopathological change of joint and spleen, downregulated the percentage of activated T cells, and upregulated naïve T cells and Treg cells in spleen. CK significantly suppressed T cell activation (as indicated by T cell proliferation, CD25 expression, and IL-2 production). In conclusion, our results suggest that CK alleviates autoimmune arthritis by suppressing T cell activation.

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